Mutant mice with visual defects may serve as a resource for the study of the function and development of the mammalian retina. Currently, over 20 different mouse mutants have been shown to have visual defects. These mutants may also serve as animal models of various human diseases, for instance Chediack Higashi syndrome, human stationary night blindness, and retinal degenerative diseases. Using monoclonal antibodies that label specific antigens, morphological and structural abnormalities may be uncovered that correlate with the functional defects in these visual mutants. Two groups of visual mutants will be studied: the retinal degeneration mutants, and the pigmentation mutants. Recently, it has become possible to selectively label mouse cones with peanut lectin and selectively label mouse rods (and not cones), with an anti-rhodopsin antibody. These two labels will allow the degenerative topography to be precisely characterized in the rd mouse, which then can be compared to the degenerative patterns found in other retinal degenerative diseases. Two pigmentation mutants have been shown to have abnormalities within their visual systems that include both morphological defects and functional (light sensitivity) defects within their retinas. Conventional morphological methods have been largely unsuccessful in finding defects in the retinas from hypopigmentation mutants. Monoclonal antibodies have the potential for being powerful tools in correlating functional defects with morphological abnormalities. For instance, using monoclonal antibodies that label specific cells such as glial vs. neuron, or different types of retinal neurons, or subtypes of retinal cells, the immunocytology of the retina in the functionally deficient mutants can be compared to the normal mouse.